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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the possibility of a drug interaction between the antilipemic agent halofenate and sulfonylureas. Twelve young, healthy men were given 1 g of tolbutamide by mouth before and after 12 days of double-blind treatment with 1 g per day of halofenate, or placebo. There was a significant increase in serum tolbutamide at eight, 10 and 12 hours (P less than 0.01) and a significant (P less than 0.01) decrease in serum glucose at one, four and six hours after halofenate treatment, but not after placebo. In a long-term, double-blind study of halofenate or clofibrate treatment of patients with Type IV hyperlipoproteinemia, diabetic patients receiving a sulfonylurea and halofenate either required a reduction in the dose of the sulfonylurea or demonstrated significantly improved control of hyperglycemia (P less than 0.05) or both. No appreciable decrease in serum glucose levels was noted in diabetic patients receiving sulfonylurea and clofibrate. This interaction between halofenate and sulfonylureas is clinically important, especially in view of the association of hyperlipemia and diabetes.
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PMID:Potentiation of hypoglycemic effect of sulfonylureas by halofenate. 17 74

In order to evaluate the importance of measuring serum lipids in the current care of diabetics, blood triglycerides were measured in 155 diabetics and 59 controls. Comparison with a chemical method confirmed the usefulness of the nephelometric method for the diagnosis and control of hyperlipemia in current practice. The importance of measuring serum lipids was confirmed by a close correlation between lipemia and cardiovascular complications such as coronary insufficiency, high blood pressure, and peripheral arterial insufficiency. It appeared also that glycemia and cholesterol are not sufficient to assess the biological pattern and prognosis of diabetes. Thus, lipemia is an essential parameter in the evaluation of any diabetic because of its value regarding prognosis and control therapy.
Acta Diabetol Lat
PMID:Usefulness of serum lipid determination in diabetic practice. 71 68

The precise pathogenesis of human diabetic kidney disease and the factors responsible for the susceptibility to it remain to be established. However, there is now evidence that renal disease clusters in families and that genetic factors are of central importance in determining liability. A predisposition to arterial hypertension has been suggested as playing a contributory role in the development of kidney disease. Genetically controlled hypertrophic processes may be implicated in the susceptibility to arterial wall damage and glomerular injury in diabetes. This suggestion derives from the observation that the fibroblasts of patients with diabetic nephropathy show a higher Na+/H+ antiport activity and a greater 3H-thymidine incorporation into DNA than fibroblasts of diabetic patients without nephropathy. The first sign of renal damage is the appearance of microalbuminuria and of a small elevation in arterial pressure, changes associated with significant mesangial expansion. Microalbuminuria is associated with abnormalities of lipoprotein profiles possibly as a consequence of insulin-resistance-induced hyperinsulinemia. It could be postulated that the environmental changes brought about by diabetes lead in susceptible individuals to increased systemic and intraglomerular pressure on the one hand and mesangial expansion on the other. These two processes would cause proteinuria and glomerulosclerosis. Lipid abnormalities would further aggravate the renal histological damage and, in combination with hypertension, contribute to the accelerated atherosclerosis typical of patients with diabetic kidney disease. A vicious circle would thus be triggered of reduction in renal function, more hypertension, more proteinuria, more glomerular obsolence, more hyperlipidemia and eventually end-stage renal failure or premature cardiovascular death.
Acta Diabetol Lat
PMID:Mechanisms of diabetic renal and cardiovascular disease. 207 90

Alternative medications for hyperlipidemia management have been continuously searched for above all because currently employed drugs appear not to be effective or are poorly tolerated. Fibers, such as guar-gum, seem to be able to reduce cholesterol levels, but their extensive and long-term use is beset by the high incidence of gastrointestinal side-effects. In this study the administration of guar-enriched pasta has proved to reduce fasting and post-prandial cholesterol levels significantly in 15 obese normocholesterolemic women (5 diabetics and 10 non-diabetics). The women reported good palatableness of guar-pasta without any side-effects.
Acta Diabetol Lat
PMID:Effects of guar-pasta on serum lipid levels in obese diabetic and non-diabetic women with normal lipids. 285 6

An association between arterial blood pressure and blood viscosity has been suggested in healthy and in diabetic subjects, and that the hemorheological pattern may be influenced by blood lipid alterations. In diabetic patients a relationship between arterial hypertension and blood lipid changes may therefore be suggested. This study concerns 19 type II diabetics with hyperlipidemia (triglycerides = 3.2 +/- 1 mmol/l; total cholesterol = 6.1 +/- 1.2 mmol/l; HDL-cholesterol = 0.92 +/- 0.27 mmol/l; VLDL = 29 +/- 5%) (group A), and 19 normolipidemic type II diabetics (triglycerides = 1.15 +/- 0.5 mmol/l; total cholesterol = 5.1 +/- 1 mmol/l; HDL-cholesterol = 1.25 +/- 0.38 mmol/l; VLDL = 20 +/- 5%) (group B). No differences concerning age, body weight, duration of diabetes and glycemic control were found in hyperlipidemic compared to normolipidemic diabetics. On the contrary, higher systolic and diastolic blood pressure levels were demonstrated in group A (167 +/- 14 mmHg and 101 +/- 5.2 mmHg, respectively) than in group B (144 +/- 15 mmHg, p less than 0.001 and 87 +/- 6.9 mmHg, p less than 0.001, respectively). An increase of plasma apolipoprotein B level (163 +/- 27 mg/dl vs 102 +/- 21 mg/dl, p less than 0.001), of plasma viscosity (1.81 +/- 0.08 mPas vs 1.51 +/- 0.07 mPas, p less than 0.001) and of blood viscosity (5.37 +/- 0.33 mPas vs 5.07 +/- 0.04 mPas, p less than 0.01, at shear-rate of 90 s-1; 18.4 +/- 1 mPas vs 14.1 +/- 0.9 mPas, p less than 0.001 at shear-rate of 2.25 s-1) was found in group A, compared to group B.(ABSTRACT TRUNCATED AT 250 WORDS)
Acta Diabetol Lat
PMID:Increased plasma apolipoprotein B levels and blood hyperviscosity in non-insulin-dependent diabetic patients: role in the occurrence of arterial hypertension. 343 3

Severe forms of arterial occlusive diseases occurred more frequently in 11 insulin-treated diabetics with persisting hyperlipidemia than in 10 control subjects who were 11 years older. Triglycerides and cholesterol of total serum and of VLDL were 2-7 times higher (P less than 0.01); however, LDL-cholesterol was 2 times lower than in control subjects (P less than 0.025). HDL-cholesterol was not significantly different in either group. After insulin administration (81 U/die vs 37 U/die, P less than 0.00251), the increased lipids were only insignificantly reduced, while LDL-cholesterol and the ratio of LDL-/HDL-cholesterol was even increased (P less than 0.0025 and P less than 0.05). In contrast to control subjects, VLDL-cholesterol was positively correlated to the tolbutamide-induced insulin reserve (before insulin administration) and to the diurnal insulin dosage (after insulin administration) (P less than 0.01 and P less than 0.001). The results show that the atherosclerotic risk in diabetics with persisting hyperlipidemia is higher than in control subjects and that the risk is distinguished by increased VLDL-cholesterol in correlation with increased insulin concentrations. Since the atherosclerotic risk is even more accentuated by the fact that insulin administration increases LDL-cholesterol, insulin therapy must be observed carefully in these patients.
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PMID:[Persisting hyperlipidemias as risk factors of diabetic macroangiopathy]. 352 28

Most traditional hypoglycemic treatments for non-insulin-dependent diabetes mellitus (NIDDM) are of considerable antiquity. What we would now call a low-carbohydrate diet was first used in 1796; insulin was introduced in 1922; the (toxic) biguanide synthalin was used sparingly from 1926 until the Second World War; and tolbutamide and chlorpropamide were marketed in the late 1950s. Amphetamine was available as an anorectic agent in the 1950s. Hence, representatives of all our present treatments for NIDDM have been available for over 30 y, but there is still great uncertainty about how to use them best. This uncertainty is reflected in major variations in prescription rates from country to country. In spite of this formidable pharmacological armamentarium, we have to face the fact that glycemic control is unsatisfactory in the majority of patients with NIDDM; irrespective of the mode of treatment, less than a quarter have a normal glycated hemoglobin. We clearly need new approaches to control glycemia in NIDDM. Furthermore, in addition to high blood glucose, many patients with NIDDM also have hypertension, hyperlipidemia, and other atherogenic abnormalities that need to be tackled if mortality (predominantly from atherosclerotic vascular disease) is to be reduced. It seems improbable that a single drug will be found to cure the many metabolic abnormalities. Polypharmacy thus seems inevitable for many patients.
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PMID:Traditional pharmacological management of non-insulin-dependent diabetes. 854 15

The structural alterations of endocardial endothelial cells of the heart right atrium and left ventricle were investigated in Golden Syrian hamsters subjected to streptozotocin-induced diabetes and to a combination of diabetes and diet-induced hyperlipidemia. Animals were examined at time intervals ranging from 2 weeks to 6 months. Anionic sites of the endothelial plasmalemma were visualized by in situ perfusion of cationized ferritin. The results indicated that: (a) both atrial and ventricular endocardial endothelium are affected in streptozotocin-induced diabetes: endothelium converts from continuous into a fenestrated type, (b) although the anionic charge of the plasmalemma decreased in advanced diabetes, the newly formed fenestrae highly bound cationized ferritin, (c) combined diabetes and hyperlipidemia induced more severe alterations of endocardial endothelium: new permeable endothelial structures were formed (transendothelial channels, open intercellular junctions, fused plasmalemmal vesicles), and the cells became particularly enriched in cytoskeleton (intermediate filaments and microtubules), (d) the thick subendocardial layer of connective tissue contained, in the combined experimental model, macrophage derived foam cells indicative for the occurrence of alterations of atherosclerotic type.
Acta Diabetol 1996 Mar
PMID:The pathomorphological alterations of endocardial endothelium in experimental diabetes and diabetes associated with hyperlipidemia. 877 84

The objective of this investigation was to determine whether calcium channel blocker (CCB) treatment effectively restores normal baseline mechanical function in diabetic myocardium and to evaluate its effect on the interval-strength relationship. Wistar rats were made diabetic with streptozotocin (55 mg/kg, IV). Left-ventricular papillary muscles from normal and diabetic (10 weeks) rats were superfused with Tyrode's solution at 30 degrees C. A subgroup of diabetic and normal animals received daily injections of verapamil or nifedipine (10 mg/kg, IP; 8 weeks) to compare the effectiveness of a phenylalkylamine to a dihydropyridine in reversing diabetes-induced contractile dysfunction in vitro. Muscles were electrically stimulated at 0.5 Hz with suprathreshold stimuli, and the following parameters were measured: peak tension developed, time to-peak tension, time-to-90% relaxation, and the maximum velocities of tension development and decay. Experimental diabetes was characterized by: severe hyperglycemia, hepatomegaly, reduced body weight gain, cardiomegaly, and increased plasma phospholipid levels. In addition, baseline values of peak tension developed, time to-peak tension, and time-to-90% relaxation were significantly greater in muscles from diabetic animals. Chronic nifedipine treatment reduced hyperglycemia and plasma phospholipid levels, normalized body weight gain, and reduced both heart and liver sizes in diabetic animals. Nifedipine treatment completely reversed diabetes-induced prolongation in both time-to-peak tension and time-to-90% relaxation. In diabetic myocardium, a slightly positive component was present in the interval-strength relationship between 0.01 and 1 Hz, resulting in a rightward shift in the entire curve across a wide range of stimulation frequencies (0.01-5 Hz). This positive component was absent in muscles from diabetic animals treated with both CCBs, and verapamil produced a leftward shift in the frequency response curve. The results of this study suggest that chronic nifedipine treatment may be more effective than verapamil in restoring normal baseline myocardial mechanical function, reducing hyperglycemia and hyperlipidemia, as well as attenuating both cardiac and liver enlargement in experimental diabetes. In contrast, verapamil treatment tended to normalize more effectively the inotropic response to changes in stimulation frequency in diabetic myocardium.
Acta Diabetol 1996 Mar
PMID:Influence of calcium channel blocker treatment on the mechanical properties of diabetic rat myocardium. 877 89

Obesity is often accompanied by non-insulin-dependent diabetes mellitus (type 2), arterial hypertension, and hyperlipidaemia. The aim of this study was to evaluate whether duration of obesity is a risk factor for the appearance of type 2 diabetes, hypertension, and hyperlipidaemia. We studied 760 obese subjects, 207 of whom had normal glucose tolerance, 125 impaired glucose tolerance, and 428 type 2 diabetes; in addition, 560 had hypertension and 315 had hyperlipidaemia. At univariate analysis, passing from normal through impaired glucose tolerance to type 2 diabetes there was a progressive increase of age and of duration of obesity, hypertension and hyperlipidaemia. Compared to subjects without hypertension, hypertensive subjects were older, had a longer duration of obesity, a greater body mass index (BMI, kg/m2), and more frequently a family history of hypertension; they also more frequently showed impaired glucose tolerance and type 2 diabetes and hyperlipidaemia. Compared to subjects without hyperlipidaemia, hyperlipidaemic subjects were older, had a longer duration of obesity, and more frequently showed impaired glucose tolerance and type 2 diabetes, and hypertension. Diabetes, hypertension, and hyperlipidaemia were highly associated, as up to 80% of subjects with type 2 diabetes had hypertension, and more than 80% of hyperlipidaemic subjects had hypertension. Type 2 diabetes was less frequent than hypertension and hyperlipidaemia during the first 10 years of obesity, and progressively increased thereafter; in contrast the frequency of hypertension and of hyperlipidaemia increased only after 30 years of obesity. In 359 subjects undergoing an oral glucose tolerance test (168 with simultaneous determination of insulin release), increasing durations of obesity were accompanied by an increasing prevalence of type 2 diabetes, and in deterioration of glucose response, with no decrease in insulin release. At logistic regression analysis, age was a common risk factor for diabetes, hypertension, and hyperlipidaemia; duration of obesity and hyperlipidaemia were additional risk factors for diabetes; family history of hypertension, BMI and hyperlipidaemia were additional risk factors for hypertension, as were impaired glucose tolerance or diabetes, and hypertension for hyperlipidaemia. These data indicate that duration of obesity is a risk factor for type 2 diabetes, and emphasize the importance of preventing obesity in young subjects.
Acta Diabetol 1998 Oct
PMID:Duration of obesity is a risk factor for non-insulin-dependent diabetes mellitus, not for arterial hypertension or for hyperlipidaemia. 984 Apr 48


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